If you go to the link the numbers are staggering. I invested in Prana because of their strong science and see huge value. I suspect most of us know someone who has been touched by this horrible disease and would like to see PBT2 work not just for the profit it would bring.
Key recommendations and conclusions
The new data has shown that the current burden and future impact of the dementia epidemic has been underestimated, particularly for the Asia East and Sub-Saharan African regions. The global burden will soon shift to poorer countries
Our best estimates show that 10% of dementia cases may be avoided by improvements in public health. Campaigns that target smoking, underactivity, obesity, hypertension and diabetes should be prioritised as well as education and other cognitive enhancement
The current economic cost of dementia is $604 billion annually (2010). These costs will escalate at least proportionally with numbers affected, particularly in low and middle income countries
Research must be a global priority if we are to improve the quality and coverage of care, find treatments that alter the course of the disease and identify more options for prevention
Investment into a search for a cure must be balanced with initiatives to improve access to evidence based packages of care
Lessons can be drawn from the HIV epidemic regarding the relationship between success in research and the presence of well-established care systems, access to diagnostic technologies and drug therapies in low and middle income countries and better implementation of ‘global trials’
Dementia must be declared a public health priority by initiating national debates regarding the future provision for long term care. So far, only 13 out of 193 WHO countries have national dementia plans in place.
All countries, not just those in the G8, must commit to comprehensive plans for collaborative action. International cooperation will be essential and there is a need for a global action plan between governments, industry and non-profit organisations like Alzheimer associations.
LONDON, December 5, 2013 /PRNewswire/ --
In a policy brief launched today, Alzheimer's Disease International (ADI) has announced that the number of people living with dementia worldwide in 2013 is now estimated at 44 million (estimated at 35 million in 2010), reaching 76 million in 2030 (66 million) and 135 million by 2050 (115 million). The Policy Brief entitled 'The Global Impact of Dementia 2013-2050' reports a staggering 17% increase in global estimates of people living with dementia, compared to the original ADI estimates in the 2009 World Alzheimer's Report.
Although high income countries like all those in G8 have borne the brunt of the dementia epidemic, the disease is a global phenomenon. In the next few decades the global burden of the disease will shift inexorably to low and middle income countries with 71% of those with dementia living in lower and middle-income countries by 2050.
Marc Wortmann, Executive Director of ADI, comments, "At the eve of the G8 Dementia Summit in London, UK, it is not just the G8 countries, but all nations, that must commit to a sustained increase in dementia research."
Professor Martin Prince, from King's College London and author of the Policy Brief, says: "The governments of the world's richest nations are focusing today upon dementia. This is a global problem that is, increasingly, impacting on developing countries with limited resources and little time to develop comprehensive systems of social protection, health and social care. While we all hope for advances in treatment that could blunt the impact of the coming epidemic, we need to agree now to work together to close the diagnosis and treatment gap. Nobody should be left without access to support and care."
Most governments are woefully unprepared for the dementia epidemic with only 13 countries implementing a national dementia plan. All governments should initiate a national dialogue regarding future provision and financing of long term care. There is an urgent need for a collaborative, global action plan for governments, industry and non-profit organisations like Alzheimer associations.
Research must become a global priority if we are to improve the quality and coverage of care, find treatments that alter the course of the disease and identify more options for prevention. Priority should be equally given to policymaking, health and social care service and health system development.
NOTES TO EDITOR
Int J Alzheimers Dis. 2013;2013:414817. Epub 2013 Oct 29.
Role of Copper and Cholesterol Association in the Neurodegenerative Process.
Arnal N, Morel GR, de Alaniz MJ, Castillo O, Marra CA.
INIBIOLP (Instituto de Investigaciones Bioquímicas de La Plata), CCT La Plata, CONICET-UNLP, Cátedra de Bioquímica y Biología Molecular, Facultad de Ciencias Médicas, Universidad Nacional de La Plata, 60 y 120 (1900) La Plata, Argentina.
Age is one of the main factors involved in the development of neurological illnesses, in particular, Alzheimer, and it is widely held that the rapid aging of the world population is accompanied by a rise in the prevalence and incidence of Alzheimer disease. However, evidence from recent decades indicates that Cu and Cho overload are emerging causative factors in neurodegeneration, a hypothesis that has been partially investigated in experimental models. The link between these two variables and the onset of Alzheimer disease has opened up interesting new possibilities requiring more in-depth analysis. The aim of the present study was therefore to investigate the effect of the association of Cu + Cho (CuCho) as a possible synergistic factor in the development of an Alzheimer-like pathology in Wistar rats. We measured total- and nonceruloplasmin-bound Cu and Cho (free and sterified) contents in plasma and brain zones (cortex and hippocampus), markers of oxidative stress damage, inflammation, and programmed cell death (caspase-3 and calpain isoforms). The ratio beta-amyloid (1-42)/(1-40) was determined in plasma and brain as neurodegenerative biomarker. An evaluation of visuospatial memory (Barnes maze test) was also performed. The results demonstrate the establishment of a prooxidative and proinflammatory environment after CuCho treatment, hallmarked by increased TBARS, protein carbonyls, and nitrite plus nitrate levels in plasma and brain zones (cortex and hippocampus) with a consequent increase in the activity of calpains and no significant changes in caspase-3. A simultaneous increase in the plasma A β 1-42/A β 1-40 ratio was found. Furthermore, a slight but noticeable change in visuospatial memory was observed in rats treated with CuCho. We conclude that our model could reflect an initial stage of neurodegeneration in which Cu and Cho interact with one another to exacerbate neurological damage.
PMID: 24288650 [PubMed - as supplied by publisher]
Experience tells us, of course, that exhorting people to eat better and exercise more often falls on deaf ears. But with obesity rates levelling off in some parts of the world and falling slightly in others, there is some evidence that the message is getting through.
If the link between diabetes and Alzheimer's is firmed up, there will be even more reason to take heed – and even more reason to keep banging the public health drum. Good news comes in many guises. The possibility that Alzheimer's is "just" diabetes is one of them.
This article appeared in print under the headline "Banish the bogeyman"
Evidence is growing that Alzheimer's could actually be a late stage of type 2 diabetes – if it is, we all have another big reason to live healthier lives
JUST over 100 years ago, German pathologist Alois Alzheimer dissected the brain of a 57-year-old woman who had died, demented, in a hospital in Kassel. He found tangles of strange fibrous deposits that seemed to have destroyed her brain from within.
Today, the disease that bears his name is a bogeyman stalking our ageing societies. About 35 million people have Alzheimer's; most of them require expensive, exhausting care. By 2050 that number is expected to triple. We still don't really know what causes the disease or how it destroys the brain. There is no way to prevent it and no cure. Dealing with the epidemic will cost trillions.
All it not lost, however. We could be in the midst of a rethink that promises to banish the bogeyman. There is growing evidence that Alzheimer's is actually a late stage of another disease, type 2 diabetes. The link between the two has been noted for a few years and though it remains a hypothesis, the evidence is growing (see "Are Alzheimer's and diabetes the same disease?").
At first glance that sounds like bad news. If the Alzheimer's epidemic is scary, the type 2 diabetes one is truly terrifying. About 270 million people have type 2 diabetes already and their ranks are swelling rapidly – among them adolescents and young adults. If they are destined to progress to Alzheimer's disease, the future looks bleak.
Or perhaps not. Type 2 diabetes is largely a lifestyle disease, caused by obesity, poor diet and lack of exercise. It can be prevented, alleviated and even cured by lifestyle changes, which holds out the hope that we could start to deal with Alzheimer's in a similar way.
Experience tells us, of course, that exhorting people to eat better and exercise more often falls on deaf ears. But with obesity rates levelling off in some parts of the world and falling slightly in others, t
J Neurosci Res. 2013 Nov 22. doi: 10.1002/jnr.23320. [Epub ahead of print]
Oxidative damage and amyloid-β metabolism in brain regions of the longest-lived rodents.
Edrey YH, Oddo S, Cornelius C, Caccamo A, Calabrese V, Buffenstein R.
Department of Physiology, University of Texas Health Science Center at San Antonio, San Antonio, Texas; The Barshop Institute for Aging and Longevity Studies, University of Texas Health Science Center at San Antonio, San Antonio, Texas.
Naked mole rats (NMRs) are the longest-lived rodents, with young individuals having high levels of Aβ in their brains. The purpose of this study was twofold: to assess the distribution of Aβ in key regions of NMR brains (cortex, hippocampus, cerebellum) and to understand whether the accumulation of Aβ is due to enhanced production or decreased degradation. Recent evidence indicates that lipid peroxides directly participate in induction of cytoprotective proteins, such as heat shock proteins (Hsps), which play a central role in the cellular mechanisms of stress tolerance. Amyloid precursor protein processing, lipid peroxidation, Hsps, redox status, and protein degradation processes were therefore assessed in key NMR brain regions. NMR brains had high levels of lipid peroxidation compared with mice, and the NMR hippocampus had the highest levels of the most toxic moiety of Aβ (soluble Aβ1 - 42 ). This was due not to increased Aβ production but rather to low antioxidant potential, which was associated with low induction of Hsp70 and heme oxygenase-1 as well as low ubiquitin-proteasome activity. NMRs may therefore serve as natural models for understanding the relationship between oxidative stress and Aβ levels and its effects on the brain. © 2013 Wiley Periodicals, Inc.
Copyright © 2013 Wiley Periodicals, Inc.
over the whole day. Rhythms in the way genes are expressed are lost."
FitzGerald uses mice lacking Bmal1 to study whether clock cells have links to diabetes and heart disease. He has shown that clock genes influence blood pressure, blood sugar and lipid levels.
Several years ago, Musiek, who at the time was a neurology resident at the University of Pennsylvania, and FitzGerald decided to investigate how knocking out Bmal1 affects the brain. Holtzman, who has published pioneering work on sleep and Alzheimer's disease, encouraged Musiek to continue and expand these studies when he came to Washington University as a postdoctoral fellow.
In the new study, Musiek found that as the mice aged, many of their brain cells became damaged and did not function normally. The patterns of damage were similar to those seen in Alzheimer's disease and other neurodegenerative disorders.
"Brain cell injury in these mice far exceeded that normally seen in aging mice," Musiek said. "Many of the injuries appear to be caused by free radicals, which are byproducts of metabolism. If free radicals come into contact with brain cells or other tissue, they can cause damaging chemical reactions."
This led Musiek to examine the production of key antioxidant enzymes, which usually neutralize and help clear free radicals from the brain, thereby limiting damage. He found levels of several antioxidant proteins peak in the middle of the day in healthy mice. However, this surge is absent in mice lacking Bmal1. Without the surge, free radicals may remain in the brain longer, contributing to the damage Musiek observed.
"We're trying to identify more specifics about how problems in clock genes contribute to neurodegeneration, both with and without influencing sleep," Musiek said. "That's a challenging distinction to make, but it needs to be made because clock genes appear to control many other functions in the brain in addition to sleeping and waking."
Nov. 25, 2013 — A new discovery may help explain the surprisingly strong connections between sleep problems and neurodegenerative conditions such as Alzheimer's disease. Sleep loss increases the risk of Alzheimer's disease, and disrupted sleeping patterns are among the first signs of this devastating disorder.
Scientists at Washington University School of Medicine in St. Louis and the University of Pennsylvania have shown that brain cell damage similar to that seen in Alzheimer's disease and other disorders results when a gene that controls the sleep-wake cycle and other bodily rhythms is disabled.
The researchers found evidence that disabling a circadian clock gene that controls the daily rhythms of many bodily processes blocks a part of the brain's housekeeping cycle that neutralizes dangerous chemicals known as free radicals."Normally in the hours leading up to midday, the brain increases its production of certain antioxidant enzymes, which help clean up free radicals," said first author Erik Musiek, MD, PhD, assistant professor of neurology at the School of Medicine. "When clock genes are disabled, though, this surge no longer occurs, and the free radicals may linger in the brain and cause more damage."Musiek conducted the research in the labs of Garret FitzGerald, MD, chairman of pharmacology at the University of Pennsylvania, and of David Holtzman, MD, the Andrew B. and Gretchen P. Jones Professor and head of the Department of Neurology at Washington University School of Medicine, who are co-senior authors.The study appears Nov. 25 in The Journal of Clinical Investigation.Musiek studied mice lacking a master clock gene called Bmal1. Without this gene, activities that normally occur at particular times of day are disrupted."For example, mice normally are active at night and asleep during the day, but when Bmal1 is missing, they sleep equally in the day and in the night, with no circadian rhythm," Musiek said. "They get the same amount of sleep, but it's spread
For all longs who have followed Pana for many years it's nice to see the light bulb go off in main stream media on PBT2's science. Finally the ah ha moment!
When Renaissance invests the other money starts to follow .. sorta like the Buffet effect.
"In 2003, we organized a round table discussion of leading scientists in the field and in related fields, at which we learned that there was a genetic basis for autism".
I suspect the fund uses the same research criteria when selecting companies to invest in. Get the most knowledge in the field.
Great interview with Jim Simons founder of Renaissance Technologies and his philanthropic work. Big interest in Autism .